Metformin Inhibition of Mitochondrial ATP and DNA Synthesis Abrogates NLRP3 Inflammasome Activation and Pulmonary Inflammation

Researchers showed that metformin inhibited NLRP3 inflammasome activation and interleukin (IL)-1β production in cultured and alveolar macrophages along with inflammasome-independent IL-6 secretion, thus attenuating lipopolysaccharide- and SARS-CoV-2-induced Acute respiratory distress syndrome.
[Immunity]
Xian, H., Liu, Y., Nilsson, A. R., Gatchalian, R., Crother, T. R., Tourtellotte, W. G., Zhang, Y., Aleman-Muench, G. R., Lewis, G., Chen, W., Kang, S., Luevanos, M., Trudler, D., Lipton, S. A., Soroosh, P., Teijaro, J., Torre, J. C. de la, Arditi, M., Karin, M., & Sanchez-Lopez, E. (2021). Metformin inhibition of mitochondrial ATP and DNA synthesis abrogates NLRP3 inflammasome activation and pulmonary inflammation. Immunity, 0(0). https://doi.org/10.1016/j.immuni.2021.05.004 Cite
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Interleukin-6 Signaling and Anti-Interleukin-6 Therapeutics in Cardiovascular Disease

Scientists provide an overview of the mechanisms by which IL-6 signaling occurs and how that impacts upon pharmacologic inhibition, and describe murine models of IL-6 and atherogenesis.
[Circulation Research]
Ridker Paul M, & Rane Manas. (n.d.). Interleukin-6 Signaling and Anti-Interleukin-6 Therapeutics in Cardiovascular Disease. Circulation Research, 0(0). https://doi.org/10.1161/CIRCRESAHA.121.319077 Cite
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Extracellular Vesicles Derived from M2 Microglia Reduce Ischemic Brain Injury through microRNA-135a-5p/TXNIP/NLRP3 Axis

Investigators explored the specific functions of M2 phenotype microglia-derived extracellular vesicles in ischemic brain injury progression.
[Laboratory Investigation]
Liu, Y., Li, Y.-P., Xiao, L.-M., Chen, L.-K., Zheng, S.-Y., Zeng, E.-M., & Xu, C.-H. (2021). Extracellular vesicles derived from M2 microglia reduce ischemic brain injury through microRNA-135a-5p/TXNIP/NLRP3 axis. Laboratory Investigation, 1–14. https://doi.org/10.1038/s41374-021-00545-1 Cite
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NLRP3 Inflammasome-Mediated Cytokine Production and Pyroptosis Cell Death in Breast Cancer

Investigators focus on the role of NLRP3 inflammasome and its components in breast cancer signaling, highlighting that a more detailed understanding of the clinical relevance of these pathways could significantly contribute to the development of novel therapeutic strategies for breast cancer.
[Journal of Biomedical Science]
Faria, S. S., Costantini, S., de Lima, V. C. C., de Andrade, V. P., Rialland, M., Cedric, R., Budillon, A., & Magalhães, K. G. (2021). NLRP3 inflammasome-mediated cytokine production and pyroptosis cell death in breast cancer. Journal of Biomedical Science, 28(1), 26. https://doi.org/10.1186/s12929-021-00724-8 Cite
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CD47-Mediated Hedgehog/SMO/GLI1 Signaling Promotes Mesenchymal Stem Cell Immunomodulation in Mouse Liver Inflammation

Investigators found that mesenchymal stem cell CD47 and macrophage signal regulatory protein alpha expression were increased after LPS stimulation.
[Hepatology]
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Soluble α-Synuclein–Antibody Complexes Activate the NLRP3 Inflammasome in hiPSC-Derived Microglia

Researchers showed that αSyn activated the NLRP3 inflammasome in human induced pluripotent stem cell (hiPSC)-derived microglia via dual stimulation involving Toll-like receptor 2 engagement and mitochondrial damage.
[Proceedings of the National Academy of Sciences of the United States of America]
Trudler, D., Nazor, K. L., Eisele, Y. S., Grabauskas, T., Dolatabadi, N., Parker, J., Sultan, A., Zhong, Z., Goodwin, M. S., Levites, Y., Golde, T. E., Kelly, J. W., Sierks, M. R., Schork, N. J., Karin, M., Ambasudhan, R., & Lipton, S. A. (2021). Soluble α-synuclein–antibody complexes activate the NLRP3 inflammasome in hiPSC-derived microglia. Proceedings of the National Academy of Sciences, 118(15). https://doi.org/10.1073/pnas.2025847118 Cite
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The Complement System Drives Local Inflammatory Tissue Priming by Metabolic Reprogramming of Synovial Fibroblasts

Scientists defined the molecular and cellular mechanisms of this inflammation-mediated tissue priming. Re-exposure to inflammatory stimuli caused aggravated arthritis in rodent models.
[Immunity]
Friščić, J., Böttcher, M., Reinwald, C., Bruns, H., Wirth, B., Popp, S.-J., Walker, K. I., Ackermann, J. A., Chen, X., Turner, J., Zhu, H., Seyler, L., Euler, M., Kirchner, P., Krüger, R., Ekici, A. B., Major, T., Aust, O., Weidner, D., … Hoffmann, M. H. (2021). The complement system drives local inflammatory tissue priming by metabolic reprogramming of synovial fibroblasts. Immunity, 0(0). https://doi.org/10.1016/j.immuni.2021.03.003 Cite
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Protectin DX Restores Treg/Th17 Cell Balance in Rheumatoid Arthritis by Inhibiting NLRP3 Inflammasome via miR-20a

Nucleotide-binding domain–like receptor protein 3 (NLRP3) knockout and rescue experiments demonstrated that NLRP3 participated in protectin DX-mediated Treg/Th17 cell balance restoration, joint injury amelioration and inflammatory-response attenuation using Nlrp3−/− mice.
[Cell Death & Disease]
Jin, S., Sun, S., Ling, H., Ma, J., Zhang, X., Xie, Z., Zhan, N., Zheng, W., Li, M., Qin, Y., Zhao, H., Chen, Y., Yang, X., & Wang, J. (2021). Protectin DX restores Treg/T h 17 cell balance in rheumatoid arthritis by inhibiting NLRP3 inflammasome via miR-20a. Cell Death & Disease, 12(3), 1–11. https://doi.org/10.1038/s41419-021-03562-6 Cite
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NLRP3 Inflammasome in Cancer and Metabolic Diseases

Scientists cover the mechanisms of NLRP3 inflammasome activation and its divergent roles in the pathogenesis of inflammation-associated diseases such as cancer, atherosclerosis, diabetes and obesity
[Nature Immunology]
Sharma, B. R., & Kanneganti, T.-D. (2021). NLRP3 inflammasome in cancer and metabolic diseases. Nature Immunology, 1–10. https://doi.org/10.1038/s41590-021-00886-5 Cite
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Itaconate Confers Tolerance to Late NLRP3 Inflammasome Activation

Scientists demonstrated major inflammatory tolerance and cell death phenotypes associated with itaconate production in activated macrophages.
[Cell Reports]
Bambouskova, M., Potuckova, L., Paulenda, T., Kerndl, M., Mogilenko, D. A., Lizotte, K., Swain, A., Hayes, S., Sheldon, R. D., Kim, H., Kapadnis, U., Ellis, A. E., Isaguirre, C., Burdess, S., Laha, A., Amarasinghe, G. K., Chubukov, V., Roddy, T. P., Diamond, M. S., … Artyomov, M. N. (2021). Itaconate confers tolerance to late NLRP3 inflammasome activation. Cell Reports, 34(10). https://doi.org/10.1016/j.celrep.2021.108756 Cite
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1,2, 4-Trimethoxybenzene Selectively Inhibits NLRP3 Inflammasome Activation and Attenuates Experimental Autoimmune Encephalomyelitis

Researchers showed that 1,2,4-TTB (1 mM) markedly suppressed nigericin- or ATP-induced NLRP3 inflammasome activation, thus decreased caspase-1 activation and IL-1β secretion in immortalized murine bone marrow-derived macrophages (iBMDMs) and in primary mouse microglia.
[Acta Pharmacologica Sinica]
1,2,4-Trimethoxybenzene selectively inhibits NLRP3 inflammasome activation and attenuates experimental autoimmune encephalomyelitis | Acta Pharmacologica Sinica. (n.d.). Retrieved March 1, 2021, from https://www.nature.com/articles/s41401-021-00613-8 Cite
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